(SC,RS)-Bromido-(N-{4-methyl-1-[(4-methyl-phenyl)sul-fan-yl]-pentan-2-yl}-N'-(pyridin-2-yl)imidazol-2-yl-idene)palladium(II) bromide.

The mol-ecule of the title NCNHCS pincer N-heterocyclic carbene palladium(II) complex, [PdBr(C21H25N3S)]Br, exhibits a slightly distorted square-planar coordination at the palladium(II) atom, with the five-membered chelate ring nearly planar. The six-membered chelate ring adopts an envelope conformation. Upon chelation, the sulfur atom becomes a stereogenic centre with an RS configuration induced by the chiral carbon of the precursor imidazolium salt. There are intra-molecular C-H⋯Br-Pd hydrogen bonds in the structure. The two inter-stitial Br atoms, as the counter-anion of the structure, are both located on crystallographic twofold axes and are connected to the complex cations via C-H⋯·Br hydrogen bonds.

Comparison of immunotoxic effects induced by the extracts from methanol and gasoline engine exhausts in vitro.

Gasoline engine exhaust has been considered as a major source of air pollution in China. Due to lower cyto- and geno-toxicity effects of methanol engine exhaust, methanol is regarded as a potential substitute for gasoline. We have previously compared cyto- and geno-toxicities of gasoline engine exhaust with that of methanol engine exhaust in A549 cells (Zhang et al., 2007).To characterize the immunotoxic effects for gasoline and methanol engine exhausts in immune cell, in this study, we further compared effects of gasoline and methanol engine exhausts on immune function in RAW264.7 cell and rabbit alveolar macrophages. Results showed that both gasoline and methanol engine exhaust could evidently inhibit RAW264.7 cell proliferation, promote RAW264.7 cell apoptosis, decrease E-rosette formation rate and inhibit anti-tumor effects of alveolar macrophages, at the same time, these effects of gasoline engine exhaust were far stronger than those of methanol engine exhaust. In addition, gasoline engine exhaust could significantly inhibit activities of ADCC of alveolar macrophages, but methanol engine exhaust could not. These results suggested that both gasoline and methanol engine exhausts might be immunotoxic atmospheric pollutants, but some effects of gasoline engine exhaust on immunotoxicities may be far stronger than that of methanol engine exhaust.

[Study on bisphenol A induced primary cultured mesencephalic neuronal cell injury by oxidative stress].

OBJECTIVE: To investigate the effect and mechanism of bisphenol A, a common EDCs, on the primary cultured mesencephalic neuronal cell injury. METHODS: mesencephalic neuronal cells were obtained from embryonic 14-15 day SD fetuses and were cultured in serum free medium for 4 or 7 days in vitro, 1,10,25,50 and 100 micromol/L bisphenol A were added to the medium and intracellular ROS, SOD, MDA, GSH were measured after 24 or 48hours, respectively. Flow cytometry was used to detect the neuronal cell apoptosis. Tyrosine hydroxylase immunohistochemistry was used to identity and count the ratio of dopaminergic neuronal cell. RESULTS: The intracellular ROS was dose dependently increased by bisphenol A in all treated groups, and it appeared to be a nonselective effect when the concentration of bisphenol A were higher than 50 micromol/L, and concomitantly decreased SOD, GSH and increased MDA. The apoptotic neuronal cells were significantly increased at 501 micromol/L and 100 micromol/L. The ratio of Tyrosine hydroxylase positive neuronal cell was dose dependently decreased with the concentration of bisphenol A. CONCLUSION: ROS induced by bisphenol A may play a major role in its cytotoxicity on dopaminergic neuronal cell.

[Adverse effects of nonylphenol on the reproductive development of F1 male SD rats in sexual maturation period].

OBJECTIVE: To investigate the adverse effects of perinatal exposure to nonylphenol (NP) on the reproductive development of F1 male SD rats in sexual maturation period. METHODS: The pregnant rats were randomly divided into control, 50 mg/kg, 100 mg/kg, and 200 mg/kg NP groups respectively. NP was administered to dams by gavage from gestation day 7 to weaning period. Rat pups were sacrificed at postnatal day 55. The concentration of serum testosterone was measured by radioimmunoassay. The epididymis was subjected to the determination of sperm count and motility while the testis was submitted to histopathological and immunohistochemical analyses. RESULTS: Compared with control, the concentration of serum testosterone, sperm count and motility in the 200 mg/kg NP dose groups significantly decreased (P < 0.05), and the histopathological examination revealed that NP-treated groups had higher rates of maldeveloped siminiferous tubules, smaller amount of Sertoli cells and weaker spermatogenesis. The expression of proliferative cell nuclear antigen (PCNA) significantly decreased in the 200 mg/kg NP dose groups (P < 0.05). The expression of Arom in 100 mg/kg and 200 mg/kg NP dose groups was lower than that in control. There was no significant difference in ER expression between the control and NP-treated groups. CONCLUSION: These findings indicated that 200 mg/kg Nonylphenol apparently damaged the reproductive development of F1 male SD rats in the sexual maturation period.

[Genotoxicity comparison between gasoline- and methanol-fueled exhaust by TK gene mutation assay].

Methanol fuel is a most promising substitute for gasoline. It is scarcely reported about methanol-fueled exhaust on the health effect, neither about genotoxicity research between methanol- and gasoline-fueled exhaust. In the present study, the two kinds of exhaust were sampled directly from tailpipe at the same type bus, the same state, L5178Y thymidine kinase (TK) gene mutation assay was used to investigate their genotoxicity at the same dose range, and compared with micronucleus and comet assay. The results showed that the genotoxicity of gasoline-fueled exhaust is stronger than that of methanol-fueled exhaust, while the cytotoxicity of methanol-fueled exhaust is stronger than that of gasoline-fueled exhaust at dose range. The study demonstrated that L5178Y TK gene mutation assay is more sensitive than micronucleus and comet assay.

[Adverse effects of nonylphenol on the reproductive function of adult male SD rats].

OBJECTIVE: To assess the adverse effects of both in vivo and in vitro exposure to nonylphenol on the reproductive function of adult male SD rats. METHODS: Adult male SD rats were sacrificed after they had received oral nonylphenol at 50, 100, 200 mg/kg for 28 days. Both indications related to their reproductive function and histopathological section of testis were analyzed. In vitro study of testicular cells from adult male rats by use of culture solution with different nonylphenol concentrations was conducted. Testosterone production in cell culture medium was examined and the ultrastructure of Leydig cell, Sertoli cell and spermatogenesis cell were observed under electron microscope. RESULTS: In vivo study of the experiment animals in comparison with the controls revealed that sperm count and motility in testis of adult rats exposed to nonylphenol at doses of 100 mg/kg and above were significantly decreased, and the histopathological sections of testis showed atrophied seminiferous tubules and decreased spermatogenesis. In vitro study of testicular cell culture showed that testosterone secretion was inhibited. And electron microscopy disclosed that the endoplasmic reticulum of Leydig cell swelled, which might indicate the reduction of testosterone biosynthesis. CONCLUSION: Nonylphenol at higher dose directly impairs the reproductive function of adult male SD rats.